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Analysis of Ca2+-triggered Ras GTPase-activating protein function

Reference	BBS/E/B/0000C197
Principal Investigator / Supervisor	Dr Simon Cook
Co-Investigators / Co-Supervisors	Professor Len Stephens
Institution	Babraham Institute
Department	Babraham Institute Department
Funding type	Research
Value (£)	649,357
Status	Completed
Type	Institute Project
Start date	27/01/2005
End date	26/01/2008
Duration	36 months

Abstract

Cells need to sense changes in their environment in order to survive and grow. An important mechanism involves the communication of a signal from the cell surface into the cell. Ras proteins are located on cell membranes and serve a critical role in receiving and decoding signals from cell surface receptors. They are binary switches, responding to receptor stimulation by switching to an active conformation that signals to effector pathways to regulate gene expression. Ras genes are mutated in human cancers and have been shown to induce changes associated with the tumorigenic state; therefore they are described as proto-oncogenes. They are mutated to an active form in up to 30% of human cancers. Understanding how the Ras switch is activated and inhibited is therefore critical for human health. We recently discovered novel inhibitors of the Ras switch called CAPRI and RASAL that promote the Ras `off state¿ in a Ca2+-dependent manner. These are Ras GTPase-activating proteins (GAPs). We wish to discover more about the intrinsic function of Ca2+-regulated GAPs by gene disruption in the mouse. This will lead to a greater understanding of the mechanisms by which Ras is regulated during receptor-stimulated Ca2+ signals.

Summary

unavailable

Committee	Closed Committee - Biochemistry & Cell Biology (BCB)
Research Topics	X – not assigned to a current Research Topic
Research Priority	X – Research Priority information not available
Research Initiative	X - not in an Initiative
Funding Scheme	X – not Funded via a specific Funding Scheme

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